Ventricular Remodeling

Ventricular Remodeling

Ventricular remodeling consists of two processes following a myocardial infarction. Initial one is infarct expansion. Later the ventricular cavity dilates and assumes a globular shape. The extent of remodeling depends on the size of the myocardial infarction. Significant remodeling does not occur in small infarcts. Progressive dilatation of the ventricle due to remodeling is detrimental to ventricular function.

Remodeling can be prevented by reducing the afterload by giving drugs like angiotensin converting enzyme inhibitors. Neurohormonal activation in heart failure contributes to the worsening of remodeling due to actual damage to uninfarcted myocardium (neurohormonal toxicity).

The concept of ventricular remodeling was introduced by Hockman and Buckey in 1982 in an experimental model of myocardial infarction [1]. They noted that none of the four exclusively non transmural infarctions had ventricular remodeling. The degree of infarct expansion correlated with infarct size and progressed as time passed.

An international consensus statement in 2000 defined cardiac remodeling as a group of molecular, cellular and interstitial changes. These in turn manifest clinically as changes in size, shape and function of the heart resulting from cardiac injury [2,3].

References

1. J S Hochman, B H Bulkley. Expansion of Acute Myocardial Infarction: An Experimental Study. Circulation. 1982 Jun;65(7):1446-50.
2. Paula S Azevedo, Bertha F Polegato, Marcos F Minicucci, Sergio A R Paiva, Leonardo A M Zornoff. Cardiac Remodeling: Concepts, Clinical Impact, Pathophysiological Mechanisms and Pharmacologic Treatment. Arq Bras Cardiol. 2016 Jan;106(1):62-9.
3. J N Cohn, R Ferrari, N Sharpe. Cardiac Remodeling–Concepts and Clinical Implications: A Consensus Paper From an International Forum on Cardiac Remodeling. Behalf of an International Forum on Cardiac Remodeling. J Am Coll Cardiol. 2000 Mar 1;35(3):569-82.